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Effects of Secretin on the Normal and Pathological β-Cell^*

BENJAMIN GLASER, BRAHM SHAPIRO, JERRY GLOWNIAK, STEFAN S. FAJANS and AARON I. VINIK

Department of Internal Medicine [Divisions of Endocrinology and Metabolism (B.G., B.S., J.G., S.S.F., A.I. V. and Nuclear Medicine (B.S.)J and the Department of Surgery (A.I.V.), University of Michigan Medical Center Ann Arbor, Michigan 48109

Address all correspondence and requests for reprints to: Aaron I Vinik, M.D., University of Michigan Medical Center, 2922B Taubman Health Center, 1500 East Medical Center Drive, Ann Arbor, Michigan 48109-0331.

Secretin is a gastrointestinal hormone that stimulates insulin secretion and enhances the insulin response to glucose. The mechanism by which secretin acts on the β-cell has not been extensively studied. The plasma insulin responses to secretin (2 U/kg), expressed as the percent increase relative to basal plasma insulin concentrations, were similar in normal (n = 23) and obese subjects with normal glucose tolerance (n = 12), but were decreased in obese subjects with abnormal glucose tolerance (n = 11). The insulin response to secretin was directly proportional to the basal insulin concentration in these three groups. The effects of secretin on β-cell function was not altered by propranolol (n = 6), atropine (n = 8), or surgical vagotomy (n = 10). Patients with single islet cell tumors secreting insulin (n = 18) had no plasma insulin response to secretin, whereas patients with noninsulin-secreting pancreatic tumors (gastrinomas; n = 6) and patients in whom single insulinomas had been removed (n = 7) responded normally. Two adult patients with multiple B-cell adenomas and hyperplasia (not associated with multiple endocrine neoplasia type I) hyperresponded to secretin, whereas patients with multiple endocrine neoplasia, type I, without hyperinsulinism responded normally. One patient with nesidioblastosis had no response to secretin, indicating that the pathophysiology of this entity is distinct from that of other forms of islet hyperplasia.

These data suggest that secretin stimulates β-cells directly rather than through cholinergic, adrenergic, or vagal peptidergic neural mechanisms. In addition, the ability to respond to secretin appears to be lost in patients with single insulinomas and nesidioblastosis, but not in those with multiple B-cell adenomas and hyperplasia. The lack of a plasma insulin response in patients with single insulinomas and the high normal or exaggerated response in patients with multiple B-cell adenomas and hyperplasia may prove useful in differentiating these entities.

^* This work was supported in part by Grants AM-07245 and 5-P60-AM-20752 from the NIDDK and 5M01-RR-42 from the Division of Research Resources, NIH.

Present address: Department of Endocrinology and Metabolism, Hadassah Medical Center, Jerusalem, Israel.

Present address: Veterans Administration Hospital, P.O. Box 1034, Portland, Oregon.

Received June 17, 1987.

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